Aging involves progressive and irreversible loss of cellular processes and physiological functions that ultimately increase the likelihood of death. Molecular correlates of aging, including an increase in chromosomal structural abnormalities, the frequency of single-strand DNA breaks, a decline in DNA methylation, and a loss of DNA telomeric sequences, have been described in a range of eukaryotic organisms from mammals, such as humans, to unicellular organisms, such as yeast.
Although several mechanisms have been postulated as mediators of aging (e.g., somatic mutation theory, error catastrophe theory, intrinsic DNA rearrangement theory), none have led to interventions or therapies to slow aging and increase life span. In humans, declining health in aging individuals has a significant impact on the cost and implementation of geriatric health care.
Thus, there is a need to identify agents which alter (e.g., agonize, antagonize) the level of substrates and cellular mediators associated with the aging process. The identification of such agents is important in the development of specific and effective treatment regimens to decrease aging or increase the life span of a cell or an organism, and to further define pathways which lead to aging in a cell or organism.